Polypropylene Microplastics Disrupt Epithelial Barrier Integrity and Viability in Human Airway Epithelial Cells

Abstract

Objective To investigate the effects of polypropylene microplastics (PP-MPs) on the integrity and viability of upper airway epithelial cells and to elucidate the underlying mechanisms. Methods Human nasal primary epithelial cells and a human alveolar epithelial cell line A549 were exposed to PP-MPs. Intracellular reactive oxygen species (ROS) production, epithelial–mesenchymal transition (EMT) markers (N-cadherin, vimentin), and tight junction (TJ) proteins (ZO-1, E-cadherin, occludin) were analyzed. Activation of the TGF-β/p38 mitogen-activated protein kinase (MAPK) signaling pathway was evaluated. In addition, the effects of the ROS scavenger N-acetyl-L-cysteine (NAC) were assessed. Results PP-MP exposure significantly increased intracellular ROS production and induced EMT, as evidenced by upregulation of N-cadherin and vimentin, along with downregulation of TJ proteins, including ZO-1, E-cadherin, and occludin. These changes were associated with activation of the TGF-β/p38 MAPK signaling pathway. NAC treatment effectively reversed these effects, restoring epithelial barrier integrity. Conclusion PP-MPs induce EMT and impair epithelial barrier function through ROS-mediated activation of the TGF-β/p38 MAPK pathway. These findings highlight the potential respiratory health risks associated with MP exposure.